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Applied and Environmental Microbiology, August 2004, p. 5005-5009, Vol. 70, No. 8
0099-2240/04/$08.00+0 DOI: 10.1128/AEM.70.8.5005-5009.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Biology, Technion-Israel Institute of Technology, Haifa 32000,1 Department of Plant Sciences, George S. Wise Faculty of Life Science, Tel Aviv University, Ramat Aviv 69978, Israel2
Received 25 January 2004/ Accepted 1 May 2004
Conserved eukaryotic signaling proteins participate in development and disease in plant-pathogenic fungi. Strains with mutations in CGA1, a heterotrimeric G protein G alpha subunit gene of the maize pathogen Cochliobolus heterostrophus, are defective in several developmental pathways. Conidia from CGA1 mutants germinate as abnormal, straight-growing germ tubes that form few appressoria, and the mutants are female sterile. Nevertheless, these mutants can cause normal lesions on plants, unlike other filamentous fungal plant pathogens in which functional homologues of CGA1 are required for full virulence.
cga1 mutants of C. heterostrophus were less infective of several maize varieties under most conditions, but not all, as virulence was nearly normal on detached leaves. This difference could be related to the rapid senescence of detached leaves, since delaying senescence with cytokinin also had differential effects on the virulence of the wild type and the
cga1 mutant. In particular, detached leaves may provide a more readily available nutrient source than attached leaves. Decreased fitness of
cga1 as a pathogen may reflect conditions under which full virulence requires signal transduction through CGA1-mediated pathways. The virulence of these signal transduction mutants is thus affected differentially by the physiological state of the host.
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